There are three basic levels of control of aging: 1) the proximate causes leading to senesence in particular cell lines or tissues, 2) the regulatory processes that integrate the cell and tissue specific patterns into an individual's life history, and 3) the evolutionary forces that select upon life history traits to determine the aging pattern characteristic of the species. In the past we have studied the control of aging at all three levels with the abnormal abdomen (aa) syndrome in Drosophila mercatorum. Recently, we have extended this integrated, multi-level approach study the aging phenotypes associated with insertion-induced bobbed (bb) flies in the closely related species, D. hydei. Aa and bb show many similarities; both are associated with homologous inserts that go into the coding region of the 28S ribosomal genes, both seem to induce a fuctional ribosomal deficiency in polytene tissue, both lead to phenotypes that appear to be due to lower activities of juvenile hormone esterase, and both are adaptive under desiccating conditions in nature because of their effects upon adult sexual maturation and longevity. Despite these many parallels, the aging effects associated with aa are controlled at the molecular level through somatic overreplication (or its failure) of noninserted 28S genes during formation of the fat body, the polytene tissue that produces the juvenile hormone esterase. In contrast, preliminary data indicate that bb in hydei is controlled by adjusting the number of inserted to noninserted 28S genes in the germ-line. By performing our studies on both species, we can not only learn how aging is controlled at several different levels of biological organization, but we also hope to ultimately answer the question as to why two such closely related species have utilized such different molecular routes to achieve similar development, physiological and ecological ends with respect to their aging patterns.